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L Vela

Publications and source records attributed to L Vela.

25 records · Page 2Linked to original sources

Platelet-activating factor antagonists do not protect against the development of experimental autoimmune encephalomyelitis.

There is evidence suggesting the involvement of the platelet-activating factor (PAF) in central nervous system (CNS) functions. The possibility exists that PAF may be relevant in eliciting cell-mediated autoimmune phenomena in CNS. To assess the role of PAF in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), male Lewis rats were primed with whole spinal cord from guinea pig, emulsified in Freund's adjuvant supplemented with 10 mg/ml of Mycobacterium tuberculosis, H37Ra strain. Treatment with two different PAF antagonists (PCA 4248, WEB 2170) was applied starting from day 1 or day 5 postinoculation on a twice-daily basis. Neither PCA 4248 nor WEB 2170 suppressed the clinical signs of EAE. PAF concentration was measured in CNS tissue from the 9th day after inoculation to the 15th day, and no differences were found between control and EAE animals. These results suggest that PAF is not involved in the mediation of EAE.

Animals↗

[Extrapontine myelinolyses caused by iatrogenic hypernatremia following rupture of a hydatid cyst of the liver with an amnesic syndrome as sequela].

INTRODUCTION: Extrapontine myelinolisis is a rare condition caused by severe hydroelectrolytic disorders. Following an initial stage of diffuse encephalopathy, the neurological sequelae are usually of diffuse cognitive deficits and extrapyramidal or cortico-bulbo-spinal disorders. We report a case of extrapontine myelinolisis following hypertonic peritoneal lavage due to rupture of a hydatid cyst of the liver (HCL), which was followed by a syndrome of isolated amnesia due to bilateral hippocampal lesions. CLINICAL CASE: Following rupture of a HCL a 37 year old man was treated by peritoneal lavage with hypertonic saline solution. In the immediate postoperative period he had a prolonged confusion state associated with natremia of 176 mg/dl, which was corrected in less than 24 hours. Seven days later the patient had an apathy-inattention frontal syndrome. Six weeks later, and lasting until three months after operation, he had a selective memory deficit in learning tests (of the Barcelona-PIENC series of tests) with normality (29/30) in the MMST. On magnetic resonance there were hyperintense images in T2 in both hippocampus, insulas and corpus callosum. CONCLUSIONS: Generally caused by rapidly corrected hyponatremia, isolated hyponatremia or hypernatremia may also lead to extrapontine myelinolisis. However, we have found no report of extrapontine myelinolisis due to rupture of HCL and treatment with hypertonic peritoneal lavage. The neurological sequelae of extrapontine myelinolisis are usually global cognitive deficits, extra-pyramidal or cortico-bulbo-spinal disorders. Lesions seen on MR are usually found in the basal ganglia, thalamus or corpus callosum (with or without involvement of the pons). We have found no descriptions of bilateral hippocampal lesions causing selective memory deficits in this condition. Treatment by hypertonic peritoneal lavage for ruptured HCL may cause severe hydro-electrolytic alterations which may lead to myelinolisis of the CNS. We report of a case with bilateral hippocampal lesions and selective memory deficit, not previously described within the clinical spectrum of extrapontine myelinolisis.

Adult↗

[Crossed apraxia secondary to a right parietal infarct].

INTRODUCTION: Crossed apraxia is an unusual alteration in praxic function due to a cerebral lesion which is contralateral to that which would be expected. We report a case of crossed apraxia due to a right parietal lesion in a left handed patient who had been obliged to be right handed. We discuss the peculiar neuropsychological profile and possible relation of this to left handedness. CLINICAL CASE: A 75 year old man, left handed but obliged to use the right hand, suffered an acute episode of alteration in the management of utensils (lids, taps, medicine containers), although he maintained his usual social behaviour and orientation. On neurosomatic examination no focal deficits were observed. On MMST he scored 29/30, on the Edinburgh questionnaire he scored 35 (left handed dominance). On a Barcelona PIENC battery his scores were in the pathological range for subtests on understanding orders, carrying out symbolic gestures and imitating gestures, in perceiving super imposed images and visual memory. MRI showed a right parietal laminar infarct. CONCLUSIONS: The patient showed clear bilateral ideo motor apraxia, which could not be justified/explained by visuo spatial agnosia secondary to a right parietal ischaemic lesion. It is usually considered that ideatory and ideomotor apraxias are due to left hemisphere lesions, whilst contsructive apraxia and apraxia related to dress are due to right hemisphere lesions. In this case, there was ideomotor apraxia secondary to a right parietal lesion, that is to say a crossed ideomotor apraxia, without crossing of other neuropsychological functions. This supports the theory of independence of hemisphere dominance for different cognitive functions. The frustrated left handedness of the patient might be related to the greater probability of unusual hemisphere dominance for ideomotor praxis function in this particular case.

Aged↗

[Is progressive anarthria a clinical form of Pick complex?].

INTRODUCTION: Progressive anarthria is defined as a clinical entity with a degenerative origin consisting in progressive difficulty in articulating while grammatical, semantic and graphic aspects of language are preserved. It is included within the group of processes affecting restricted areas of the brain although its exact nosological location is not clear. We report two cases that progressed clinically towards frontotemporal dementia and corticobasal degeneration, respectively. CASE REPORTS: Case 1: a male who, at the age of 72, began with speech difficulties while comprehension and reading/writing skills were preserved. Three years later he developed apathy, bulimia, sexual indiscretions and aggressiveness, with preservation of visual memory, visual-constructional capacity and elementary writing skills. Case 2: a male who, at the age of 70, began with speech disorders, which were associated two years later to generalised slowness with Hoehn and Yahr stage II akinetic-rigid symptoms; another two years later, he developed a dystonic attitude and melokinetic apraxia in the left upper limb. CONCLUSIONS: The two cases, which were initially compatible with progressive anarthria, progressed clinically towards frontotemporal dementia and corticobasal degeneration, which are entities that are included in 'Pick complex'. This is a concept that we believe to be useful from a clinical point of view, given the variability that exists in the histology of the entities that have been proposed as members of this syndrome group, together with the progression of the cases described in the literature and the ones we have reported in this work.

Aged↗

[Management and improvement of the process of outpatient treatment of transient ischemic attacks in Neurology departments].

AIMS: To describe our experience in the ambulatory treatment of transient ischemic attacks (TIA) in a second-level hospital with the implementation of an example of process management within the different services involved in attending such conditions. PATIENTS AND METHODS: The following aspects of the process--mission, limits, flowchart, eligibility criteria and performance indicators (process, sentinel and effectiveness)--were defined by multidisciplinary consensus (Emergency, Vascular Surgery, Cardiology, Neurology and Radiology departments). This process was implemented from April 2002 to May 2004, and monthly assessments were carried out to check for problems and to introduce corrective measures. After ending the process, patients with TIA were admitted as inpatients for a hospital study. RESULTS: Definition of the process: medical care (diagnosis and treatment) of TIA patients who are eligible for a complete outpatient study within seven days. Patients evaluated: 254. Indicator 1 (percentage of suitable referrals): 2002: 53%, 2003: 75%, 2004: 73%. Indicator 2 (percentage of complete studies in less than one week): 2002: 35%, 2003: 57%, 2004: 50%; hospitalised: 90%. Indicator 3 (infarcts during the study): 2002: 4.3%, 2003: 0%, 2004: 0%; hospitalised: 0%. Indicator 4 (percentage of adjustments made to treatment): 2002: 39%, 2003: 31%, 2004: 62%; hospitalised: 72%. Mean delay before visit: in February 2002: 90 days, in April 2002: 7.67 days and in April 2003: 5.37. Problems detected: delays in referrals, failure to fit hospitalisation criteria, delays in carrying out examinations not included in the protocol, unsuitable indicator design. Steps taken: redefinition of indicators, modification of the referral system, adjustments made to the circuits involved in carrying out tests, review of hospitalisation criteria. CONCLUSIONS: Process management is an ideal tool for achieving ongoing improvements in clinical praxis. Early monitoring makes it possible to detect problems and to implement corrective measures. In our area, the study of TIA must be performed in a hospital inpatient regimen in order to comply with the guidelines for clinical practice.

Ambulatory Care↗